As awareness of erosion and the impact thereof increases among dental practitioners and patients, there is a need for approaches to correctly diagnose the source of erosion and identify individuals with heighted susceptibility to erosion. Unlike caries, which produce deep localized subsurface lesions due to prolonged exposure to bacterial acids, erosion results from dissolution and softening of the entire enamel surface from short and frequent exposures to low pH dietary acids, leading to softening and micron-scale mineral loss especially when followed by brushing with abrasive toothpastes. Dietary acids like citric acid are particularly damaging due to not only their acidic pH, but also their calcium-chelating capacity, which drives further enamel dissolution.
The acquired enamel pellicle (AEP) naturally provides some protection against acid attack on enamel. The AEP contains calcium and phosphate ions as well as proteins and enzymes. Pellicle formation is a complex, multi-step process in which precursor proteins like statherin and proline-rich proteins bind initially and provide binding sites for additional proteins (mucins, etc). Maturation involves cross-linking and dephosphorylation of pellicle proteins and binding of plaque bacteria in later stages after 2 hours. The composition of the pellicle is highly dependent on saliva content which varies with flow rate, stimulation, time of day, diet, etc. Salivary flow rate greatly impacts saliva pH, ionic components and buffering capacity.
Erosion can result from several conditions—frequent exposure to dietary acids, gastric acids or lack of sufficient saliva (xerostomia). Patients suffering from gastric erosion are normally identified through assessment of the severity and location of the erosive damage (upper palatal surfaces), while those with xerostomia are identified by visual inspection of the saliva and measurement of salivary flow rates. There is a link between erosion and increased intake of acidic drinks, lower salivary flow rate and lower salivary pH/buffer capacity resulting from the lower salivary flow rates. However, some patients with normal salivary flow rates and no signs of gastric acid exposure still suffer from dietary erosive damage, even when exposure to dietary acids is minimized, suggesting a heightened susceptibility to erosion, potentially related to their AEP. There is a need for a simple and reliable method to identify this subset of highly susceptible patients for proper treatment, as well as to identify patients for clinical studies evaluating the effects of oral care actives to reduce, mitigate and control dental erosion from dietary acids.